The hyperlipidemia of human pregnancy consists of a 3-fold increaee in triglyceride and quarter-fold rises in phospholipids and cholesterol. The pregnant rat is a good study model for this condition. On the basis of measurements of post-heparin lipolytic activity and tissue lipoprotein lipases, we hypothesize that this physiological adaptation serves to enhance delivery of circulating fat to appropriate tissues. In midgestation, one appropriate tissue is the body fat store where lipoprotein lipase activity is increased. In late gestation, the appropriate removal sites may be elsewhere, including placenta and mammary tissue, as adipose tissue lipoprotein lipase activity is greatly reduced. An overproduction of lipoprotein triglyceride probably complements these changes in removal. In vitro and in vivo studies to test these ideas directly are underway in the pregnant rat, a model system we have thoroughly characterized. A possible autoregulatory control of triglyceride removal by apoprotein alterations in pregnancy is also under study. Finally, while the lipemia of pregnancy is assumed to be physiologic, we are establishing a clearer definition of normal and abnormal as well as pathophysiological correlations in the abnormal group.